Trophoblast-Induced Changes in C-X-C Motif Chemokine 10 Expression Contribute to Vascular Smooth Muscle Cell Dedifferentiation During Spiral Artery Remodeling

Wallace, Alison E.; Cartwright, Judith E.; Begum, Runa; Laing, Ken; Thilaganathan, B.; Whitley, Guy

doi:10.1161/atvbaha.112.300354

Cited by 37 publications

(33 citation statements)

References 54 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These data suggest that only the WT mice showed transient changes in VSMC subtype expression during collateral vessel maturation (arteriogenesis), a phenomenon not occurring in CXCL10 −/− mice. This points to a role of CXCL10 in the regulation of VSMC phenotype switch, already described by Wallace et al 23 Our data showed that CXCL10 stimulated migration of VSMCs in vitro. Furthermore, knockdown of CXCL10 by siRNA in VSMCs and HUVECs resulted in reduced VSMC migration, indicating that CXCL10 is both intrinsically and extrinsically involved in VSMC migration.…”

Section: Discussionsupporting

confidence: 88%

Absence of Chemokine (C-X-C Motif) Ligand 10 Diminishes Perfusion Recovery After Local Arterial Occlusion in Mice

Borne¹,

Haverslag²,

Brandt³

et al. 2014

ATVB

View full text Add to dashboard Cite

Objective— In arteriogenesis, pre-existing anastomoses undergo enlargement to restore blood flow in ischemic tissues. Chemokine (C-X-C motif) ligand 10 (CXCL10) is secreted after Toll-like receptor activation. Toll-like receptors are involved in arteriogenesis; however, the role of CXCL10 is still unclear. In this study, we investigated the role for CXCL10 in a murine hindlimb ischemia model. Approach and Results— Unilateral femoral artery ligation was performed in wild-type (WT) and CXCL10 −/− knockout (KO) mice and perfusion recovery was measured using laser-Doppler perfusion analysis. Perfusion recovery was significantly lower in KO mice compared with WT at days 4 and 7 after surgery (KO versus WT: 28±5% versus 81±13% at day 4; P =0.003 and 57±12% versus 107±8% at day 7; P =0.003). Vessel measurements of α-smooth muscle actin–positive vessels revealed increasing numbers in time after surgery, which was significantly higher in WT when compared with that in KO. Furthermore, α-smooth muscle actin–positive vessels were significantly larger in WT when compared with those in KO at day 7 (wall thickness, P <0.001; lumen area, P =0.003). Local inflammation was assessed in hindlimb muscles, but this did not differ between WT and KO. Chimerization experiments analyzing perfusion recovery and histology revealed an equal contribution for bone marrow–derived and circulating CXCL10. Migration assays showed a stimulating role for both intrinsic and extrinsic CXCL10 in vascular smooth muscle cell migration. Conclusions— CXCL10 plays a causal role in arteriogenesis. Bone marrow–derived CXCL10 and tissue-derived CXCL10 play a critical role in accelerating perfusion recovery after arterial occlusion in mice probably by promoting vascular smooth muscle cell recruitment and maturation of pre-existing anastomoses.

show abstract

Section: Discussionsupporting

confidence: 88%

Absence of Chemokine (C-X-C Motif) Ligand 10 Diminishes Perfusion Recovery After Local Arterial Occlusion in Mice

Borne¹,

Haverslag²,

Brandt³

et al. 2014

ATVB

View full text Add to dashboard Cite

show abstract

“…The maternal-fetal interface is a specific chemokine-rich environment and several chemokines have been found there (He et al 2012, Wallace et al 2013. Our previous work provided evidence that trophoblasts are an important source of CCL24 in human early pregnant uterus (Li et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Meng

Shang

et al. 2015

Reproduction

View full text Add to dashboard Cite

Chemokine CCL24, acting through receptor CCR3, is a potent chemoattractant for eosinophil in allergic diseases and parasitic infections. We recently reported that CCL24 and CCR3 are co-expressed by trophoblasts in human early pregnant uterus. Here we prove with evidence that steroid hormones estradiol (E), progesterone (P), and human chorionic gonadotropin (hCG), as well as decidual stromal cells (DSCs) could regulate the expression of CCL24 and CCR3 of trophoblasts. We further investigate how trophoblast-derived CCL24 mediates the function of trophoblasts in vitro, and conclude that CCL24/CCR3 promotes the proliferation, viability and invasiveness of trophoblasts. In addition, analysis of the downstream signaling pathways of CCL24/CCR3 show that extracellular signal-regulated kinases (ERK1/2) and phosphoinositide 3-kinase (PI3K) pathways may contribute to the proliferation, viability and invasiveness of trophoblasts by activating intracellular molecules Ki67 and matrix metallopeptidase 9 (MMP9). However, we did not observe any inhibitory effect on trophoblasts when blocking c-Jun N-terminal kinase (JNK) or p38 pathways. In conclusion, our data suggests that trophoblast-derived CCL24 at the maternal-fetal interface promotes trophoblasts cell growth and invasiveness by ERK1/2 and PI3K pathways. Meanwhile, pregnancy-related hormones (P and hCG), as well as DSCs could up-regulate CCL24/CCR3 expression in trophoblasts, which may indirectly influence the biological functions of trophoblasts. Thus, our results provide a possible explanation for the growth and invasion of trophoblasts in human embryo implantation. Reproduction (2015) 150 417-427

show abstract

“…Differently from EO-PE, which is considered to arise primarily due impaired placental development (23), LO-PE develops at the third trimester due to the limited capacity of maternal metabolism to cope with the needs of the growing placenta and fetus (37, 38). The pathophysiology of PE involves various mechanisms being strongly implicated by renal dysfunction and renin angiotensin system (14, 15, 39). We hypothesize that elevated STC1 level during LO-PE might act as a compensatory mechanism to impair renal function and in some degree it might be modulated by the STC1 genetic variants.…”

Section: Discussionmentioning

confidence: 99%

“…In vitro studies have associated STC1 expression to angiogenesis (14) and remodeling of the spiral arteries within the maternal uterus (15), processes crucial for developing and maintaining normal pregnancy. Our seminal study showed that human STC1 gene exhibits distinct placental gestational dynamics (11).…”

mentioning

confidence: 99%

Stanniocalcin-1 Hormone in Nonpreeclamptic and Preeclamptic Pregnancy: Clinical, Life-Style, and Genetic Modulators

Juhanson

Rull

Kikas

et al. 2016

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

Context and Objectives:The study represents the first comprehensive analysis of Stanniocalcin-1 (STC1) hormone in human pregnancy, assessing clinical, lifestyle, and genetic determinants of circulating STC1 at term.Design, Setting, and Participants:Participants included women with (n = 50) and without (n = 316) preeclampsia (PE) at delivery, recruited in the REPROgrammed fetal and/or maternal METAbolism (REPROMETA) study (2006–2011, Estonia). Genetic association analysis combined PE cases (n = 597) and controls (n = 623) from the REPROMETA and Finnish Genetics of Preeclampsia Consortium (2008–2011) studies.Main Outcome Measure(s):Maternal postpartum plasma STC1 was measured by ELISA (n = 366) and placental STC1 gene expression by TaqMan quantitative RT-PCR (n = 120). Genotyping was performed using Sequenom MassArray.Results:Significantly higher STC1 plasma level was measured for the PE (median, 1952 pg/mL; 1030–4284 pg/mL) compared with non-PE group (median, 1562 pg/mL; 423–3781 pg/mL; P = 3.7 × 10−4, Mann-Whitney U test). Statistical significance was enhanced after adjustment for cofactors (linear regression, P = 1.8 × 10−6). STC1 measurements were negatively correlated with maternal smoking. Prepregnancy body mass index had a positive correlation with STC1 only among PE patients (r = 0.45; P = .001). The strongest genetic association with hormone concentrations was detected for STC1 single nucleotide polymorphisms rs3758089 (C allele: minor allele frequency, 5%; linear regression: β = 249.2 pg/mL; P = .014) and rs12678447 (G allele: minor allele frequency, 7%; β = 147.0 pg/mL; P = .082). rs12678447 placental genotypes were significantly associated with STC1 gene expression (P = .014). The REPROMETA/Finnish Genetics of Preeclampsia Consortium meta-analysis suggested an increased risk to develop late-onset PE for the rs12678447 G allele carriers (P = .05; odds ratio = 1.38 [0.98–1.93]).Conclusions:Increased STC1 hormone represents a hallmark of late-onset PE. STC1 gene variants modulate placental gene expression and maternal hormone levels.

show abstract

Trophoblast-Induced Changes in C-X-C Motif Chemokine 10 Expression Contribute to Vascular Smooth Muscle Cell Dedifferentiation During Spiral Artery Remodeling

Cited by 37 publications

References 54 publications

Absence of Chemokine (C-X-C Motif) Ligand 10 Diminishes Perfusion Recovery After Local Arterial Occlusion in Mice

Absence of Chemokine (C-X-C Motif) Ligand 10 Diminishes Perfusion Recovery After Local Arterial Occlusion in Mice

Chemokine CCL24 promotes the growth and invasiveness of trophoblasts through ERK1/2 and PI3K signaling pathways in human early pregnancy

Stanniocalcin-1 Hormone in Nonpreeclamptic and Preeclamptic Pregnancy: Clinical, Life-Style, and Genetic Modulators

Contact Info

Product

Resources

About